Models were intended to generate preliminary mechanistic and toxicity …

Models were intended to generate preliminary mechanistic and toxicity information while reducing animal use andAndres et al. BMC Neuroscience 2013, 14:49 http://www.biomedcentral.com/1471-2202/14/Page 8 ofFigure 6 Effect of 10 M RA on K+-evoked [3H]-glycine release in M17 cells. M17 neuroblastoma cells were grown and treated with or without 10 M RA for 72 hours to induce differentiation. The treated M17 cells were then incubated with 2Ci/mL of [3H] glycine for 30 min and then stimulated with 80 mM KCl. The glycine release/Total release was then calculated. ** Significantly different from control on corresponding day after Student's t-test (pNelfinavir (Mesylate) the presence of RA for several days [11,14]. These properties make the M17 cell line a good in vitro cell model formechanistic and neurotoxicity testing. However, the functional changes in M17 cells due to RA differentiation have not been thoroughly characterized. A very relevant question is why do we need a differentiated neuronal model for neurobiology studies. The answer is that most of the neuronal functions such as membrane excitability, ion channels, neurotransmitter release, endocyctotic and exocyctotic events etc. are characteristics of mature neurons and cannot be studied in an immature neuronal model. Treatment with RA results in the progressive development of neuronal morphologies and formation of neuronal networks seen in a more PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/17139194 mature neuronal culture over time. A commonly measured characteristic of differentiation is extension of neurites that are akin to the axons and dendrites of fully differentiated neurons [33]. These neuronal properties in RA differentiated M17 cells were evidenced by both light mi.